Effect of selenium depletion on thyroidal type-I iodothyronine deiodinase activity in isolated human thyrocytes and rat thyroid and liver

The effects of dietary selenium deficiency on hepatic and thyroidal type I iodothyronine deiodinase (ID-I) and selenium-dependent glutathione peroxidase (GPx) activities have been studied in weanling rats. In selenium-deficient animals hepatic ID-I activity was reduced to 11% of the activity found in the selenium-replete groups, whilst thyroidal ID-I activity increased by 42%. Hepatic and thyroidal GPx activities were also reduced by selenium deficiency to approximately 0.6 and 70%, respectively, of the values found in the selenium-replete animals. We have also studied the effects of thyrotropin (TSH), and selenium supply on the activity of IDI and GPx in human thyrocytes grown in primary culture. When thyrocytes were grown in selenium-deficient (< 1 nmol l–1 Se) medium in the absence of TSH, addition of sodium selenite up to 1000 nmol l–1 had little or no effect on ID-I activity. In the absence of added selenite, TSH addition produced a significant increase in ID-I activity and this stimulation was increased further when selenite was added at concentrations of 50–1000 nmol l–1 with an optimal effect on ID-I activity being observed at a 500 nmol l–1. Selenium content and GPx activity in human thyrocytes grown in selenium-free media (selenium content < 1 nmol l–1) were not significantly lower than the corresponding measurements made in cells grown in media containing selenium at a concentration of 5.4 nmol l–1. These data show that thyroidal ID-I activity can be stimulated in vivo and in vitro when selenium supply for GPx synthesis is limited and support the view that in selenium deficiency the thyroid, but not the liver, is able to retain sufficient amounts of the trace element to allow continued expression of ID-I and GPx, with ID-I receiving a preferential supply of selenium. Low selenium supply is an important mediator of hepatic but not thyroidal ID-I expression.